Page 151 - Recognizing axial spondyloarthritis - Janneke de Winter

cohorts as the Pre-SpA cohort, the SPACE cohort, GESPIC and the DESIR cohort, are essential. And, referring to Figure 1, the position of a biomarker in the disease process should be considered when testing and evaluating biomarkers. Since the a priori chance of having axial SpA increases lower down the process, the study setting should be well-defined to mimic the real-life setting as close as possible. 2) The diagnostic arsenal has expanded with techniques enabling the early detection of axial SpA, such as MRI of the SI joints. A two-sided development, since on the one hand inflammation shown on MRI of the SI joints precedes structural damage and thus enables an early diagnosis, and on the other hand the current definition of an MRI of the SI joints suggestive for axial SpA lacks specificity. This calls both for redefining the definition of a positive MRI of the SI joints as well as for restraint in using MRI in the diagnostic process. Physicians should ask for diagnostic MRI of the SI joints only in patients in whom there is a moderately high suspicion of axial SpA, and should always consider other, more likely diagnoses.
The recognition of the preclinical phase of axial SpA is emerging. Boosted by recent developments in early and preclinical RA research, initiatives as the Pre- SpA cohort might prove a valuable tool to identify, stratify and describe the early and preclinical disease state, both prospectively as well as retrospectively and both clinically as well as translationally. Building on these developments, when individuals at truly increased risk are identified, treating them in a very early phase might delay or even prevent disease onset.
Together with all these developments in the early axial SpA field should come awareness. Awareness, that 1) diagnosing earlier and being more sensitive in making a diagnosis should not imply compromising on specificity. Patients are possibly over-diagnosed and over-treated (49). This potential ‘collateral damage’ should be weighed against the profits of earlier diagnosis and diagnosis of less severe and obvious disease subtypes. Treatment recommendations should be reformed to that purpose, since the current SpA nomenclature and treatment guidelines do not justify the differentiation in disease stage. 2) Although several SpA subtypes are phenotypically similar, to define one disease includes more than only the phenotype. The goal should not be to be as inclusive as possible, since phenotypically identical diseases might differ in pathobiology and thus respond differently to treatment. Homogeneous disease groups are of major importance in therapeutic trials: otherwise treatment effects could be diluted and therapeutic options that are promising could be wrongly discarded. Future research should focus on detailed profiling of axial SpA subgroups based on pathobiology. This might result in subgroups that are driven predominantly TNF driven, predominantly IL-17 driven or driven by both or other cytokines. Additionally, defining subgroups characterized by inflammation and/or by new bone formation would aid targeted treatment strategies. The novel finding of HLA-C*07 might appear useful to define those subgroups.
GENERAL DISCUSSION AND SUMMARY
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